Flaviviruses Flashcards

1
Q

Where was yellow fever most prevalent

A

when the panama canal was getting constructed

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2
Q

How was yellow fever transmitetd

A

by mosquities
aedes egypti

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3
Q

how did people discover how yellow fever was getting transmitted

A

they recruited volunteers and paid them

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4
Q

what is the type of virus of yellow fever

A

flaviviruses

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5
Q

What put an end to human experiments

A

clara maass a nurse that got paid for be bitted by yellow fever mosquitoes and she got killed

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6
Q

Mosquito brigades

A
  • Colonel Gorgas arrived in Panama as the Chief Medical Officer (1904)
  • Discoveries linking mosquitos with malaria
  • Decides to act on possibility that insects could be transmitting yellow fever
  • In 1905: “mosquito brigades”
    -campaign to fumigate and eradicate the disease
  • By Aug 1906, there were just 7 cases of yellow fever along the Panama canal
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7
Q

Control of yellow fever

A

In 1915, the Rockefeller Foundation funded a project to eliminate breeding places for Aedes aegypti in areas where yellow fever was prevalent

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8
Q

why was yellow fever nor eradicated?

A

-transmission cycle is complicated
-humans get the disease from mosquitoes
-there is a third reservoir: monkeys

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9
Q

facts about the flaviviridae family

A
  • Flavus (Latin = yellow)
  • type virus: YFV
  • Enveloped viruses
  • Icosahedral capsid
  • 40-60 nm in diameter
  • Genome: (+) ssRNA
  • monopartite, linear
  • 9.6 -12.3 kb in length
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10
Q

JEV is part of which virus fam

A

flaviviridae

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11
Q

true or false: JEV is transmitted by mosquitoes

A

true

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12
Q

Hosts of JEV

A
  • Primary hosts: birds, pigs
  • Incidental/dead-end hosts: humans
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13
Q

Symptoms of JEV

A
  • Symptoms: fever, headache, vomiting,
    neurologic symptoms (mental status,
    movement disorders, etc)
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14
Q

true or false: there is a vaccine for JEV

A

true

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15
Q

Encephalitis Viruses facts

A
  • Majority are asymptomatic or cause
    nonspecific febrile illness
  • Primarily affects children or young adults
    (0-15 yrs old) but west nile is older people
  • More severe cases:
  • Meningoencephalitis
  • Aseptic meningitis
  • Polio-like acute flaccid paralysis
  • “Parkinsonian” syndromes (tremor,
    cogwheel rigidity, masklike facies)
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16
Q

how can you get west nile

A

culex mosquitos

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17
Q

host of west nile

A
  • Primary hosts: birds
  • Incidental/dead-end hosts: humans, other
    mammals
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18
Q

who gets west nile virus

A

Primarily elderly/immunocompromised

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19
Q

symptoms of west nile virus

A

Symptoms: fever, headache, vomiting, muscle
weakness, lower back pain, neurologic symptoms (loss
of motor function, encephalitis, meningitis)

20
Q

true or false: the is no vaccine for west Nile virus

21
Q

true or false: most of the cases of west nile are symptomatic

A

false they are mostly asymptomatic

22
Q

How can you get dengue

A

Arbovirus, transmitted by
Aedes mosquitos (Aedes
aegypti and Aedes albopictus)

23
Q

What are the primary host of dengue

24
Q

symptoms of dengue

A

Fever, headache,
vomiting, abdominal pain, low
blood pressure, tachycardia,
seizures, encephalitis

25
True or false: there are no vaccines for dengue
true
26
True or false: mostly kids get dengue
false there is no age distingtion
27
How many subtypes of dengue are there and how are they spreaded our
there are four and they are all spreaded out over the world
28
where is zika the most prevalent?
in south america
29
how is zika spreaded
Arbovirus, transmitted by Aedes mosquitos (primarily Aedes aegypti)
30
What are the symptoms of zika
Symptoms (20%): fever, maculopapular rash, headache, joint and muscle plain, edema, vomiting
31
when was the last outbreak of zika and what happenend
Recent outbreaks (2013- Present): Guillain-Barré syndrome and fetal microcephaly
32
True or false: there is no vaccine for zika
true
33
what are the necessities to tackle an emerging virus
-model systems -diagnostics -vector control -therapeutic strategies
34
true or false: flavivirus encode for a polyproteins
true
35
which +ssrna virus had an immature and a mature configuration
flavivirus
36
Virus entry: flavivirus
* E protein mediates attachment to receptor * in late endosome, low pH —> E protein conformational change * sticks into endosomal membrane * results in fusion
37
What does facilitate flavivirus replications
genome circularizatio
38
what is the ration of + and - strand during replication?
there is always more + strands that are being made than - strands
39
Flavivirus replication results in sfrnas
* produced by XRN1 stalling on RNA knots in 3’UTR * inhibit antiviral responses in both hosts * type I IFN response in mammals * RNAi pathway in mosquitos * modulate cytopathic effects and cell death in mammals
40
what is srn-1
host exonuclease that degrades uncapped RNA
41
How did flaviviruses have to adapt to 2 hosts
* ie. conserved deletions in DENV 3’UTR upon mosquito- adaptation * disrupts one of the XRN1- resistant structures * leads to different primary sfRNA species * increased fitness in mosquitos, reduced in humans * reversion of deletions when re-adapted to humans
42
Infection involves a diverse population of viruses: flavivirus mutations
-the virus mutates a lot * flavivirus RdRp’s introduce 1 mutation per new strand on average * each new host/tissue/cell type will create different selective pressures * ie. in mosquitos: * virus must first escape gut * virus must eventually enter salivary glands
43
True or false: flavivirus replication induces vps and cms
* DENV induces rough-ER- derived vesicle packets (VPs) and convoluted membranes (CMs) * Sites of replication * Vesicles have pores (presumed exit site for newly synthesized viral RNAs)
44
Flavivirus assembly sites
* Budding viruses can be observed next to the pores of VPs * Virions stack within the lumen of the VP- containing ER network * Virions egress through the Golgi
45
how does flavivirus matures
the host furin will cleave the PrM into the M protein so that it is able to fuse with the host membrane
46
DENV Antibody-dependent Enhancement
* Increased severity of secondary infections * Antibodies from 1º infection recognize different serotypes weakly and facilitate DENV binding and internalization - Leukocytes and BBB cells (= encephalitis) - Inflammation and cytokine secretion (cytokine storm) - Compromises CNS function